Infection by ascospores of Sclerotinia selerotiorum caused hypersensitivity in epidermal cells in leaves and etiolated hypocotyls of bean and soybean. In bean, phaseollin and phaseollidin accumulated in leaves but kievitone alone in hypocotyls. In soybean, no phytoalexins were detected in leaves but glyceollin accumulated in hypocotyls.
Mycelial infection caused water-soaked spreading lesions in leaves and etiolated hypocotyls of both hosts. In bean, no phytoalexins were detected in leaves but kievitone alone accumulated in hypocotyls. In soybean, glyceollin accumulated in leaves but was not sought in hypocotyls.
Transfer of bean hypocotyls infected with mycelium from 18 to 28°C caused lesion limitation and marked accumulation of phaseollin and kievitone.
Phaseollin, kievitone and glyceollin inhibited ascospore germination and growth of hyphae from preformed germ-tubes and established mycelia, phaseollin being most active and glyceollin least active. Hyphal growth from mycelia was least affected by the phytoalexins.